Skip to main content

This is a preprint.

It has not yet been peer reviewed by a journal.

The National Library of Medicine is running a pilot to include preprints that result from research funded by NIH in PMC and PubMed.

medRxiv logoLink to medRxiv
[Preprint]. 2022 Apr 13:2022.04.12.22273802. [Version 1] doi: 10.1101/2022.04.12.22273802

Different HMGCR-inhibiting statins vary in their association with increased survival in patients with COVID-19

Megan M Sperry, Tomiko Oskotsky, Ivana Marić, Shruti Kaushal, Takako Takeda, Viktor Horvath, Rani K Powers, Melissa Rodas, Brooke Furlong, Mercy Soong, Pranav Prabhala, Girija Goyal, Kenneth E Carlson, Ronald J Wong, Idit Kosti, Brian Le, James Logue, Holly Hammond, Matthew Frieman, David K Stevenson, Donald E Ingber, Marina Sirota, Richard Novak
PMCID: PMC9016655  PMID: 35441166

Summary

Background

In response to the challenge to rapidly identify treatment options for COVID-19, several studies reported that statins, as a drug class, reduce mortality in these patients. Here we explored the possibility that different statins might differ in their ability to exert protective effects based on computational predictions.

Methods

A Bayesian network tool was used to predict drugs that shift the host transcriptomic response to SARS-CoV-2 infection towards a healthy state. Drugs were predicted using 14 RNA-sequencing datasets from 72 autopsy tissues and 465 COVID-19 patient samples or from cultured human cells and organoids infected with SARS-CoV-2, with a total of 2,436 drugs investigated. Top drug predictions included statins, which were tested in Vero E6 cells infected with SARS-CoV-2 and human endothelial cells infected with a related OC43 coronavirus. A database containing over 4,000 COVID-19 patients on statins was also analyzed to determine mortality risk in patients prescribed specific statins versus untreated matched controls.

Findings

Simvastatin was among the most highly predicted compounds (14/14 datasets) and five other statins were predicted to be active in > 50% of analyses. In vitro testing of SARS- CoV-2 infected cells revealed simvastatin to be a potent inhibitor whereas most other statins were less effective. Simvastatin also inhibited OC43 infection and reduced cytokine production in endothelial cells. Analysis of the clinical database revealed that reduced mortality risk was only observed in COVID-19 patients prescribed a subset of statins, including simvastatin and atorvastatin.

Interpretation

Different statins may differ in their ability to sustain the lives of COVID-19 patients despite having a shared target and lipid-modifying mechanism of action. These findings highlight the value of target-agnostic drug prediction coupled with patient databases to identify and validate non-obvious mechanisms and drug repurposing opportunities.

Funding

DARPA, Wyss Institute, Hess Research Fund, UCSF Program for Breakthrough Biomedical Research, and NIH

Full Text Availability

The license terms selected by the author(s) for this preprint version do not permit archiving in PMC. The full text is available from the preprint server.


Articles from medRxiv are provided here courtesy of Cold Spring Harbor Laboratory Preprints

RESOURCES